Toll Like Receptor Adaptor Molecule 2 (TICAM2) Antibody

Este producto es parte de TICAM - TIR domain containing adaptor molecule
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286€ (100 µl)

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935106861
info@markelab.com
name
Toll Like Receptor Adaptor Molecule 2 (TICAM2) Antibody
category
Primary Antibodies
provider
Abbexa
reference
abx104101
tested applications
WB, IHC, IF/ICC

Description

Polyclonal Antibody to Toll Like Receptor Adaptor Molecule 2 (TICAM2).

Documents del producto

Instrucciones
Data sheet
Descargar

Product specifications

Category
Primary Antibodies
Immunogen Target
Toll Like Receptor Adaptor Molecule 2 (TICAM2)
Host
Rabbit
Reactivity
Human
Recommended Dilution
WB: 0.01-2 µg/ml, IHC: 5-20 µg/ml, IF/ICC: 5-20 µg/ml. Optimal dilutions/concentrations should be determined by the end user.
Clonality
Polyclonal
Conjugation
Unconjugated
Purification
Purified by antigen-specific affinity chromatography, followed by Protein A affinity chromatography.
Size 1
100 µl
Size 2
200 µl
Size 3
1 ml
Form
Liquid
Tested Applications
WB, IHC, IF/ICC
Buffer
0.01 M PBS, pH 7.4, containing 0.05% Proclin-300, 50% glycerol.
Availability
Shipped within 5-7 working days.
Storage
Aliquot and store at -20°C. Avoid repeated freeze/thaw cycles.
Dry Ice
No
Alias
MyD88-4, TICAM-2, TIRAP3, TIRP, TRAM, toll like receptor adaptor molecule 2
Background
Antibody anti-TICAM2
Status
RUO

Descripción

TICAM2, also known as TRAM (TRIF-related adaptor molecule), is an adaptor protein that functions specifically in Toll-like receptor 4 (TLR4) signaling. It facilitates MyD88-independent pathways, mediating the activation of IRF3 and NF-κB to induce type I interferon and pro-inflammatory cytokine production. TICAM2 acts as a bridge between TLR4 and TICAM1, enabling signaling responses to lipopolysaccharides (LPS) and other pathogen-associated molecular patterns (PAMPs) in Gram-negative bacterial infections. TICAM2 is expressed primarily in immune and epithelial cells, where it contributes to early innate immune responses. Dysregulation of TICAM2 impairs TLR4-mediated IFN-β production and inflammatory signaling, leading to defective immune responses to bacterial infections or chronic inflammation in certain conditions. Knockout studies reveal a loss of MyD88-independent signaling, reduced IRF3 activation, and increased susceptibility to bacterial infections, underscoring its specific and essential role in TLR4 signaling pathways.

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